The impact of replication stress on replication dynamics and DNA damage in vertebrate cells. Técher, H., Koundrioukoff, S., Nicolas, A. Integrating old and new paradigms of G1/S control. Restriction point regulation at the crossroads between quiescence and cell proliferation. Lethality to human cancer cells through massive chromosome loss by inhibition of the mitotic checkpoint. New detailed insights into cell cycle control mechanisms and their role in cancer reveal how these dependencies can be best exploited in cancer treatment. Continuous rounds of division, however, create increased reliance on other cell cycle control mechanisms to prevent catastrophic levels of damage and maintain cell viability. Cancer-associated mutations that perturb cell cycle control allow continuous cell division chiefly by compromising the ability of cells to exit the cell cycle.
Checkpoints can delay cell cycle progression or, in response to irreparable DNA damage, induce cell cycle exit or cell death. Cell cycle checkpoints operate as DNA surveillance mechanisms that prevent the accumulation and propagation of genetic errors during cell division. Cell division is tightly regulated by multiple evolutionarily conserved cell cycle control mechanisms, to ensure the production of two genetically identical cells. Cancer is a group of diseases in which cells divide continuously and excessively.
